Knupp C J, Uner A H, Korthas C, Gavalchin J
Department of Medicine, SUNY-Health Science Center, Syracuse 13210.
Clin Immunol Immunopathol. 1993 Sep;68(3):273-82. doi: 10.1006/clin.1993.1128.
A family of nephritogenic antibodies bearing an idiotype, IdLNF1, has been shown to be important in the pathogenesis of autoimmune glomerulonephritis in the (NZB x SWR)F1 hybrid, SNF1. Previously, we have reported that a significant shift in the ratio of CD4+ to CD8+ IdLNF1-specific T lymphocytes, in favor of CD4+ IdLNF1-specific T cells, occurred at 20 to 24 weeks of age in the SNF1 and correlated with an increase in serum IdLNF1+ IgG and deposition of IdLNF1 Ig in the kidney glomeruli. Six IdLNF1-specific CD3+CD4+CD8- T cells clones have been derived from 22-week-old SNF1 mice. All six proliferated in response to Con A and anti-CD3. Three of the clones reacted with monoclonal antibody for V beta 8.1,8.2: B3, B5, and TA5 and proliferated specifically in response to IdLNF1 Ig in an Ia-restricted manner. The other three clones, A1, B6, and D2, reacted with anti-V beta 17a+ monoclonal antibody and appeared to be not Ia-restricted. T cell clones B6, D2, and TA5 promoted the production of very high levels of IdLNF1+ IgG by SNF1 B cells in vitro, while B3 and B5 induced the production of only low levels. Interestingly, clone A1 did not induce any IdLNF1+ Ig production. Furthermore, these T cell clones did not induce the production of anti-DNA antibody by SNF1 B cells.
已证明，携带个体基因型IdLNF1的一族致肾炎抗体在（NZB×SWR）F1杂交小鼠SNF1的自身免疫性肾小球肾炎发病机制中起重要作用。此前我们报道，在SNF1小鼠20至24周龄时，CD4⁺与CD8⁺IdLNF1特异性T淋巴细胞的比例发生显著变化，有利于CD4⁺IdLNF1特异性T细胞，这与血清IdLNF1⁺IgG增加及IdLNF1 Ig在肾小球中的沉积相关。已从22周龄的SNF1小鼠中获得6个IdLNF1特异性CD3⁺CD4⁺CD8⁻T细胞克隆。所有6个克隆均对刀豆蛋白A和抗CD3有增殖反应。其中3个克隆与Vβ8.1、8.2的单克隆抗体反应：B3、B5和TA5，并以Ia限制的方式对IdLNF1 Ig特异性增殖。另外3个克隆A1、B6和D2与抗Vβ17a⁺单克隆抗体反应，似乎不受Ia限制。T细胞克隆B6、D2和TA5在体外促进SNF1 B细胞产生非常高水平的IdLNF1⁺IgG，而B3和B5仅诱导低水平的产生。有趣的是，克隆A1未诱导任何IdLNF1⁺Ig的产生。此外，这些T细胞克隆未诱导SNF1 B细胞产生抗DNA抗体。
